Asano S, Honda T, Goshima F, Nishiyama Y, Sugiura Y
Department of Ophthalmology, Research Institute for Disease Mechanism and Control, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, 466-8550, Nagoya, Japan.
Neurosci Lett. 2000 Nov 17;294(2):105-8. doi: 10.1016/s0304-3940(00)01554-8.
Possible roles of the US3 gene of the herpes simplex virus (HSV) in the interaction between the virus and primary afferent neurons were examined. Neuronal apoptosis was observed in the trigeminal ganglion of mice that were infected with the wild-type (wt) of HSV-2 strain 186 and with US3-deficient mutant virus (L1BR1). In wt virus-infected mice, many HSV-immunoreactive (HSV-ir) cells were seen throughout the trigeminal ganglion, although no apoptotic change was detected. On the other hand, HSV-ir cells in L1BR1-infected mice were found only in the ophthalmic division of the trigeminal ganglions. Examination by HSV-immunohistochemistry combined with the terminal deoxynucleotidal transferase (Tdt)-mediated deoxyuridin 5'-triphosphate (dUTP) nick-end labeling (TUNEL) method showed that DNA fragmentation had occurred in almost all HSV-ir cells in the L1BRI-infected ganglion. Ultrastructurally, many viral particles were detected in apoptotic ganglionic neurons of mice infected with L1BR1. These results indicate that US3 protein kinase (US3pk) played a role in protecting HSV-infected primary afferent neurons from apoptotic cell death. The present study suggests that US3pk plays a role when HSV establishes latent infections in the sensory ganglia.
研究了单纯疱疹病毒（HSV）的US3基因在病毒与初级传入神经元相互作用中的可能作用。在感染了野生型（wt）HSV-2 186株和US3缺陷型突变病毒（L1BR1）的小鼠三叉神经节中观察到神经元凋亡。在野生型病毒感染的小鼠中，尽管未检测到凋亡变化，但在整个三叉神经节中可见许多HSV免疫反应性（HSV-ir）细胞。另一方面，在L1BR1感染的小鼠中，HSV-ir细胞仅在三叉神经节的眼支中发现。通过HSV免疫组织化学结合末端脱氧核苷酸转移酶（Tdt）介导的脱氧尿苷5'-三磷酸（dUTP）缺口末端标记（TUNEL）方法检查发现，在L1BRI感染的神经节中，几乎所有HSV-ir细胞都发生了DNA片段化。超微结构上，在感染L1BR1的小鼠凋亡神经节神经元中检测到许多病毒颗粒。这些结果表明，US3蛋白激酶（US3pk）在保护HSV感染的初级传入神经元免于凋亡性细胞死亡中发挥了作用。本研究表明，当HSV在感觉神经节中建立潜伏感染时，US3pk发挥了作用。
